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Glutathione and glutathione S-transferase in benign and malignant prostate cell lines and prostate tissues

A T Canada1, K M Roberson, R L Vessella

  • 1Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA.

Biochemical Pharmacology
|January 12, 1996
PubMed

Insights

Glutathione (GSH) and glutathione S-transferase (GST) levels differ between prostate cancer cell lines and tissues. These differences suggest established cell lines may not accurately model in vivo prostate cancer, impacting alkylator chemotherapy research.

Area of Science:

  • Oncology
  • Biochemistry
  • Pharmacology

Background:

  • Metastatic prostate adenocarcinoma shows poor response to alkylator chemotherapy.
  • Glutathione (GSH) and glutathione S-transferase (GST) are implicated in tumor resistance.
  • Limited studies compare GSH and GST in prostate cancer cell lines versus tissues.

Purpose of the Study:

  • To determine and compare GSH content and GST activity in various prostate cancer models.
  • To assess the relevance of established cell lines for in vivo prostate cancer research.
  • To identify appropriate models for improving alkylator chemotherapy efficacy.

Main Methods:

  • Quantified GSH content and GST activity in benign prostate tissues, primary and metastatic prostate adenocarcinoma tissues, immortal cell lines, and primary cell cultures.
  • Utilized a human prostate tumor xenograft (LuCaP23) in nude mice for comparison.
  • Compared in vitro cell line data with in vivo tissue and xenograft data.

Main Results:

  • Immortal cell lines exhibited higher GSH content but lower GST activity compared to fresh tissues and primary cultures.
  • Prostate tissues and primary cultures showed similar GSH content and GST activity.
  • Xenograft models demonstrated GSH and GST levels comparable to human prostate tissues.

Conclusions:

  • Significant biochemical differences exist between established prostate cancer cell lines and actual tumor tissues.
  • In vitro findings from established cell lines may not accurately predict in vivo responses to alkylator chemotherapy.
  • Prostate tissue, primary cultures, and xenografts are more suitable models for studying alkylator resistance and developing new therapeutic strategies.

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